NURSING MANAGEMENT OF ADULTS WITH DISORDERS OF THE LIVER

1. NURSING MANAGEMENT OF ADULTS WITH DISORDERS OF THE LIVER 2009

2. TOPICS TO BE REVIEWED HEPATITIS CIRRHOSIS STEATOHEPATITIS (FATTY LIVER) HEPATIC ABSCESS LIVER TRAUMA CANCER OF LIVER LIVER TRANSPLANT

3. NORMAL FUNCTION OF LIVER MAIN FUNCTIONS OF THE LIVER: storage, protection, metabolism Maintains normal serum glucose levels Ammonia conversion Protein metabolism Fat metabolism Vitamin and Iron storage Drug metabolism and detoxification

4. LIVER FUNCTION: GLUCOSE METABOLISM What happens to glucose in the liver? Where is it stored? When is it released? What is gluconeogenesis? When does it take place?

5. LIVER FUNCTION: AMMONIA CONVERSION When gluconeogenesis takes place what is the byproduct of the process? What happens to the byproduct? What do the bacteria in the intestines produce as a byproduct? How is this byproduct removed?

6. LIVER FUNCTION:PROTEIN METABOLISM What is the liver’s job in terms of synthesizing plasma proteins? What does the liver need to complete it’s job?

7. LIVER FUNCTION: FAT METABOLISM What is the liver’s job in terms of fat metabolism? When does the liver do this? What are the results of this metabolism used for?

8. LIVER FUNCTION: VITAMIN & IRON STORAGE Stores which fat soluble vitamins? What other vitamins are stored in the liver? What are these vitamins responsible for? Which minerals are stored in the liver?

9. LIVER FUNCTION: DRUG METABOLISM and DETOXIFICATION THE FOLLOWING CLASSIFICATION OF DRUGS ARE METABOLIZED BY THE LIVER? What else is metabolized by the liver? What does the liver do in terms of detoxification?

10. NORMAL FUNCTION: bile secretion What is the liver’s job with Bile? When is bile secreted? Where is Bile collected and stored? How is this related to Billirubin? When do Billirubin levels increase?

11. LIVER FUNCTION: PROTECTION What does the liver’s protection function involve? What do the cells do?

12. LIVER FUNCTION CONTINUED Inactivates Hormones Estrogen Testoterone Progesterone Aldosterone cortisol Sinusoids store blood (about 200-400 cc)

13. DISORDER OF THE LIVER HEPATITIS

14. Hepatitis Widespread viral inflammation of liver cells Hepatitis A (HAV) Hepatitis B (HBV) Hepatitis C (HCV) Hepatitis D (HDV) Hepatitis E (HEV) Hepatitis F and G are uncommon (HFV, HGV) DRUG INDUCED HEPATITIS Occurs as a secondary infection

15. Hepatitis A (HAV) Similar to that of a typical viral syndrome; often goes unrecognized Spread via the fecal-oral route by oral ingestion of fecal contaminants Contaminated water, shellfish from contaminated water, food contaminated by handlers infected with hepatitis A Also spread by oral-anal sexual activity (Continued)

16. Hepatitis A (HAV)(Continued) Incubation period for hepatitis A is 15 to 50 days. Disease is usually not life threatening. Disease may be more severe in individuals older than 40 years of age. Many people who have hepatitis A don’t know it; symptoms are similar to a gastrointestinal illness.

17. Hepatitis B (HBV) Spread is via unprotected sexual intercourse with an infected partner, sharing needles, accidental needle sticks, blood transfusions, hemodialysis, maternal-fetal route. Symptoms occur in 25 to 180 days after exposure; symptoms include anorexia, nausea and vomiting, fever, fatigue, right upper quadrant pain, dark urine, light stool, joint pain, and jaundice. (Continued) S&PS&P

18. Hepatitis B (HBV) (Continued) Hepatitis carriers can infect others, even if they are without symptoms.

19. Hepatitis C (HCV) Spread is by sharing needles, blood, blood products, or organ transplants (prior to 1992), needle stick injury, tattoos, intranasal cocaine use. Incubation period is 21 to 140 days. Most individuals are asymptomatic; damage occurs over decades. Hepatitis C is the leading indication for liver transplantation in the U.S. NOT TRANSMITTED BY CAUSUAL OR INTIMATE HOUSEHOLD CONTACT S&PS&P

20. Hepatitis D (HDV) Transmitted primarily by parenteral routes Incubation period 14 to 56 days HDV coinfects with HBV and needs it presence to replicate S&PS&P

21. Hepatitis E (HEV) Present in endemic areas where waterborne epidemics occur and in travelers to those areas (India, Asia, Africa, Middle East, Mexico, Central America & South America) Also seen in travellers coming from these areas Transmitted via fecal-oral route Resembles hepatitis A Incubation period 15 to 64 days S&PS&P

22. Clinical Manifestations of all Hepatitis Abdominal pain Changes in skin or eye color Arthralgia (joint pain) Myalgia (muscle pain) Diarrhea/constipation Wgt loss Hepatomegaly Fever Lethargy/Malaise Nausea/vomiting Intolerance to fats/dyspepsia Pruritus CHANGES IN COLOR OF URINE AND STOOL

23. ASSESSMENT HEALTH HISTORY Suspected exposure Medical history SIGNS/SYMPTOMS Pre-icteric stage Icteric stage Post-icteric stage

24. SIGNS/SYMPTOMS PRE-ICTERIC STAGE Lasts about 1 week

25. SIGNS AND SYMPTOMS ICTERIC STAGE Lasts 2-6 weeks Jaundice appears Yellow skin, sclera, mucous membranes Dark amber urine Clay colored stools

26. SIGNS AND SYMPTOMS POST-ICTERIC STAGE Lasts 2-6 weeks Jaundice subsides Liver decreases in size Good appetite

27. LABORATORY TESTS FOR HEPATITIS There will be an increase of liver enzymes and serologic markers INDICATING A PRESENCE OF HEPATITIS A, B, C

28. LABORATORY TESTS FOR HEPATITIS A (HAV) Presence of hepatitis A in client: when hepatitis A (HAV) antibodies (anti-HAV) are found in the blood Presence of immunoglobulin M(IgM) antibodies means that ongoing inflammation of liver present (persisits for 4-6 wks) Previous infection indicated by presence of immunoglbulin G (IgG) antibodies which provides permanent immunity to disease

29. LABORATORY TESTS FOR HEPATITIS B (HBV) Serologic markers which indicate client has Hepatitis B (HBV) are: HBsAg (Hepatitis B surface Antigen) Anti-HBc IgM (IgM antibodies to hepatitis B core antigen) If these levels are elevated after 6 months: chronic or carrier state Presence of antibodies to HBsAb (hepatitis B surface antibody): indicates recovery and immunity to hepatitis B Someone immunized will have a positive HBsAb

30. LABORATORY TESTS FOR HEPATITIS C (HCV) ELISA (enzyme linked immunosorbent assay ) SCREENS INITIALLY & for HCV antibodies (anti-HCV): can detect antibodies in 4 wks RIBA: (recumbent immunoblot assay): used to confirm that client has been exposed and has developed antibody HCV PCR (HCV polymerase chain reaction test): confirms presence of circulating active virus

31. LABORATORY TEST FOR HEPATITIS D (HDV) Presence of virus confirmed by identification of intrahepatic delta antigen Also by rise in hepatitis D virus antibodies (anti-HDV) titer Found within a few days of infection

32. LBORATORY TESTS FOR HEPATITIS E (HEV) VIRUS CANNOT BE DETECTED Presence of hepatitis E antibodies (anti-HEV) is found in people infected with virus

33. LABORATORY TESTS CONTINUED A person having a previous infection is indicated by immunoglobulin G (IgG) antibodies. They persist in blood and provide permanent immunity to HAV

34. LABORATORY TESTS INDICATING HEPATITIS TESTS WHICH ARE LOWERED: Leukocytes (leukopenia) Serum albumin Serum glucose (hypoglycemia) PT (prolonged) TESTS WHICH ARE ELEVATED: serum bilirubin Bilirubin in urine ALT AST Alkaline phosphatase elevated or may be normal

35. Nonsurgical Management Physical rest Psychological rest Drug therapy includes: Antiemetics Antiviral medications Immunomodulators Corticosteroids DECREASE # MEDS TO ALLOW LIVER TO REST

36. DRUGS ANTIVIRALS: Lamivudine (Epivir-HBV) Adefovir dipivoxil (Hepsera) USED: to destroy Hepatitis B virus in chronic disease SIDE EFFECTS: alters renal function; granulocytopenia

37. DRUGS IMMUNOMODULATING DRUGS: Interferon(peginterferon alfa-2a) (Pegasys) Oral ribavirin (Virazole)

38. NURSING CARE Diet therapy Hydration No alcohol Low fat, moderate protein, high CHO diet, high calorie Small frequent meals Vit B, C, K

39. PATIENT EDUCATION Prevention to health care professionals Knowledge of transmission routes Proper personal hygiene and good sanitation Gamma Globulin Avoid sex until antibody results (negative) Hepatitis A Vaccine Hepatitis B vaccine No vaccine for Hepatitis E Hepatitis C mainly spread through blood transfusions: (screen blood products)

40. CIRRHOSIS DEFINED Chronic Degenerative Causes liver enlargement Causes loss of normal liver function

41. PATHOPHYSIOLOGY Fibrotic bands of connective tissue change the structure of the liver Inflammation causes degeneration and destruction of liver cells Tissue becomes nodular Nodules block bile ducts and normal blood flow throughout the liver Blood flow changes occur from compression by the fibrous tissue

42. TYPES OF CIRRHOSIS Laennec’s cirrhosis: chronic ETOH, nutritional deficiencies Biliary Postnecrotic cirrhosis: hepatic necrosis Cardiac: congestion and tissue damage due to heart failure

43. ETIOLOGY Known causes of liver disease include: Alcohol Viral hepatitis Autoimmune hepatitis Steatohepatitis Drugs and toxins Biliary disease (Continued)

44. ETIOLOGY CONTINUED Metabolic/genetic causes Cardiovascular disease

45. EARLY SIGNS AND SYMPTOMS CIRRHOSIS Same for all types regardless of the cause Start out vague, like flu General weakness, Fatigue Anorexia, Indigestion Abnormal bowel function (constipation, or diarrhea) Abdominal pain/liver tenderness

46. LATE S & S Jaundice, pruritus, dry skin, warm bright red palms of hands (palmar erythema), rashes Edema, ascites, significant wgt change, peripheral dependent edema extremities and sacrum Bleeding tendencies/Anemia/petecchiae, echymosis Infections Menstrual irreg/gynecomastia/impotence Renal failure/dark amber urine Clay colored stools

47. ASSESSMENT INSPECTION: Jaundice Caput medusae: dilated abd veins, striae, spider angiomas Contour of abdomen: Distension: massive ascites Everted umbilicus (umbilicus protrusion) HEPATOMEGALY, SPLENOMEGALY

48. Other Physical Assessments Assess nasogastric drainage, vomitus, and stool for presence of blood Fetor hepaticus (breath odor) Amenorrhea Gynecomastia, testicular atrophy, impotence Neurologic changes: changes in LOC, leading to coma, Asterixis

49. HOW TO ELICIT ASTERIXIS Have client extend the arm, dorsiflex the wrist Extend the fingers OBSERVE rapid non-rhythmic extensions and flexions

50. Laboratory Assessment AST: Aminotransferase serum levels and LDH: lactate dehydrogenase may be elevated from hepatic cell destruction. Alkaline phosphatase levels may increase from obstructive jaundice. Total serum bilirubin from hepatic disease and urobilinogen levels may rise from hepatocellular obstruction or liver disease. decrease. (Continued)

51. Laboratory Assessment (Continued) Fecal urobilinogen is decreased due to obstructive liver disease Total serum protein and albumin levels decreased Prothrombin time prolonged; platelet count low Decreased hemoglobin and hematocrit values due to anemia and white blood cell count S&PS&P

52. LABORATORY ASSESSMENT CONTINUED Elevated ammonia levels: liver cannot excrete ammonia BUN and Serum creatinine level possibly elevated due to decreased renal function

53. COMPLICATIONS: PORTAL HYPERTENSION Increase pressure in portal vein Comes from obstruction of blood flow from pressure by CT bands (see patho) New channels looked for Blood flows back to spleen (splenomegaly) Veins become dilated (esophagus, stomach, intestines, abdomen, rectum)

54. PORTAL HYPERTENSION (CONTINUED) Results in: Ascites Esophageal varices Prominent abdominal veins (caput medusae) hemorroids

55. COMPLICATION: ASCITES DEFINED AS: Accumulation of free fluid within the peritoneal cavity With increased hydrostatic pressure from portal hypertension fluid leaks into peritoneal cavity Albumin in fluid hypoalbuminemia